Naringenin alleviates hepatic injury in zinc oxide nanoparticles exposed rats: impact on oxido-inflammatory stress and apoptotic cell death.

Human exposure to nanoparticles became unavoidable secondary to their massive involvement in a multitude of industrial applications. Zinc oxide nanoparticles (ZnONPs) are one of the most commonly used metal oxide nanoparticles in biological applications. Naringenin (NAR), a citrus-derived flavonoid, has favorable biological properties that promote human health. The present study was carried out to investigate the possible defensive role of NAR versus ZnONPs provoked hepatic injury in rats through an evaluation of liver enzymes, hepatic biomarkers of oxidative stress, inflammatory process, apoptotic cell death along with histopathological examination of liver tissue. Therefore, 32 adult rats were randomly divided into four equal groups as control, NAR, ZnONPs and co-treated ZnONPs with NAR groups. All treatments were administered for 14 days. Our results showed that ZnONPs induced hepatic injury as documented by the marked increased in hepatic enzymes activities, disturbed hepatic oxidant/antioxidant balance, increased hepatic inflammatory reactions, in addition to, extensive hepatic morphological alterations, marked collagen fibers accumulation as well as overexpression of apoptotic BAX and the noticeable intensified positive nuclear staining for nuclear factor Kabba-b in hepatic tissues. Concurrent NAR supplement to ZnONPs- treated rats significantly declined liver enzymes activities, restored oxidant/antioxidant balance, reversed inflammation, induced fewer collagen fibers accumulation, and antagonized BAX-mediated apoptotic cell death in hepatic tissues. We concluded that concurrent NAR supplement to ZnONPs treated rats improved hepatic function and structure by its antioxidant, anti-inflammatory and antiapoptotic potentials.